Genomic Fluidity of the Human Gastric Pathogen Helicobacter pylori

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Genomic fluidity associated with Helicobacter pylori has important consequences for clinical management of the gastroduodenal diseases caused by colonization with this significant pathogen. This chapter discusses the attributes of the genomes of different Helicobacter strains and the roles of strain-specific genes from the genomic plasticity region. Researchers analyze two core genome data sets, one at the genus level and the other at the species level. Helicobacter genomes were compared at the biochemical level, based on the presence of enzymes in their metabolic pathway. The Helicobacter genome was found to be subdivided into two clades, highlighting the fact that they have two distinct modes of biochemical transformation. It would be very interesting if such varied metabolic repertoires indeed represent genomic fluidity across these two Helicobacter clades. In H. pylori, three types of genomic islands coding for the type IV secretion system were identified: (i) the cytotoxin-associated gene pathogenicity island (cagPAI), (ii) the competence island (comB gene cluster), and (iii) the plasticity zone. Geneticists think that the comB transformation apparatus has evolved conservatively in H. pylori and is typically present in all the strains. This conservation explains why genomic fluidity in H. pylori is so common, especially when the deletions and rearrangements due to natural transformation and transposition are described as frequently occurring phenomena. H. pylori-induced chronic gastritis is a definitive risk factor for the development of gastric cancer.